AB0524 RELATIONSHIP BETWEEN SERUM URIC ACID, CARDIOVASCULAR RISK AND INFLAMMATORY STATUS IN PRIMARY SJÖGREN’S SYNDROME
Authors: A. Alunno, F. Carubbi, F. M. Mariani, M. Rossi, J. Santilli, C. Ferri
Journal: Annals of the Rheumatic Diseases (2022)

Background An unhealthy diet, with or without impaired renal urate excretion, is the most frequent cause of hyperuricemia. Despite its pivotal role in the pathogenesis of gout, the clinical relevance of serum uric acid (SUA) levels goes well beyond the simple association with gout and/or nephrolithiasis. Several studies pointed to hyperuricemia as cardiovascular (CV) risk factor in the general population therefore, the 2018 guidelines of the European Society of Cardiology and the European Society of Hypertension included the assessment of uricemia among the screening tests to be performed in hypertensive patients. Furthermore, in view of the association between hyperuricemia and mortality (both CV and all-cause) and CV events, it is conceivable that cardiovascular damage begins with much lower levels of uricemia. In this context, the first results of the URRAH (Uric Acid Right for Heart Health) study identified a uricemia threshold value of 4.7 mg/dL for all-cause mortality and 5.6 mg/dL for CV mortality 1 . Objectives Since patients with primary Sjögren’s syndrome (pSS) have a higher risk of CV events compared to the general population, we aimed to explore how uricemia correlates with other CV risk factors and previous CV events in patients with pSS and without gout. Methods A cross sectional study was conducted recruiting consecutive patients with pSS without history of gout. SUA was measured upon recruitment alongside the assessment of disease activity (EULAR Sjögren’s syndrome disease activity index, ESSDAI and ClinESSDAI), patient reported symptoms (EULAR Sjögren’s syndrome patient reported symptoms, ESSPRI), CV risk factors including hypertension and diabetes among others, and previous CV events. Dietary habits were also explored with various food frequency questionnaires. Results One hundred and three patients with pSS were enrolled. SUA levels ranged between 2.9 and 6.8 mg/dl and, according to the cut-off values of the URRAH study, 16 (16%) patients had SUA levels &gt;4.7 mg/dL while 5 (5%) had SUA levels &gt;5.6 mg/dL. Patients with SUA levels &gt;4.7 mg/dL were more likely males (20% vs 3%) with a higher number of CV risk factors compared to patients with SUA levels &lt;4.7mg/dL. No differences were observed regarding dietary habits across groups. Disease activity assessed with both ESSDAI and ClinESSDAI was significantly higher in patients with SUA levels &gt;4.7 mg/dL compared to patients with SUA levels &lt;4.7 (9.3 vs 6.3 p= 0.04 and 9.0 vs 6.0 p=0.03). Conversely, patient reported symptoms (total ESSPRI and individual VAS scales for total dryness, xerostomia, xerophtalmia, pain and fatigue) did not differ across groups. Logistic regression analysis confirmed the association of SUA values &gt;4.7 mg/dL and a higher number of CV risk factors (OR 2.8; 95% CI=1.2-6.5; p=0.016). Conclusion Accumulating evidence highlights the emerging role of hyperuricemia as an independent CV risk factor, but no data are available in pSS patients. This is the first study demonstrating that SUA levels &gt;4.7 mg/dL correlate with both a higher number of CV risk factors and a higher disease activity in pSS patients. Large interventional studies are needed to clarify the possible benefits of urate-lowering treatments in pSS patients. References [1]Virdis A et al. Identification of the Uric Acid Thresholds Predicting an Increased Total and Cardiovascular Mortality Over 20 Years. Hypertension 2020;75(2):302-308 Disclosure of Interests None declared